Conventional guinea pigs fed a solution of 5% w/v degraded carrageenan developed ulcerations of the cecum and large intestine within 30 days. Similar lesions were not detected in germfree guinea pigs treated in an identical manner, suggesting that an intestinal microflora was necessary for development of ulcerations. In an effort to simplify the bacterial flora required for production of ulcerations, pools consisting of ten bacterial strains each were isolated from the cecal microflora of carrageenan treated animals. Germfree guinea pigs were associated with various pools by orogastric intubation and observed for ulcer development. Animals associated with two of the ten pools tested were found to develop cecal ulcerations when fed a 5% carrageenan solution. These two bacterial pools were characterized by the presence of a cytopathic effect for WI-38 cells, collagenase activity and increased chemotactic activity as compared to the other bacterial pools. The observation that ulcerogenic pools had several factors in common which were not present in non-ulcerogenic pools led to a re-examination of human stool for similar factors. Stool samples were obtained from patients with ulcerative colitis (UC) and other inflammatory bowel diseases and from guinea pigs with carrageenan-induced colitis. Samples were extracted using the Folch procedure and were analyzed by gas liquid chromatography and a chemotactic assay. Stools from patients without UC and normal guinea pigs showed only trace amounts of long chain fatty acids (LCFA) and no chemotactic activity (CA). Both UC patient stool and carrageenan fed guinea pig stool were characterized by the presence of LCFA, with peaks corresponding to the C16 and C18 region. The LCFA fraction obtained from stool was highly chemotactic for polymorphonuclear leukocytes at concentrations of 2ng, despite the presence of less than 1% protein. Less than 1% of the material was carbohydrate, and no KDO or heptose were detected.